re^3 what cells does hiv infect??
Ralph M Bernstein
ralph at ccit.arizona.edu
Fri Apr 14 09:21:10 EST 1995
ok, derya posted:"
> I think an important point to remember is that, cell activation appears
>to be necessary for HIV-1 integration and viral replication. T cells which are
>positively selected in the thymus are presumably in the resting phase
actually, thymocytes are probably one of _the_most rapidly dividing cells in
the body. since positive selection goes on more than once in a t cell's
life (and cd4 cd8 arent always a part of that + sel) we need specifics? but
anyway, alot of cells are made in the thymus and are dividing, including
when theyre dp. it's true that alot of cells _dont_ make it out of the
thymus -thru benign neglect and negative selection, ect- but thats later,
after the dp stage.
>(though >it wasreported that mature T cells in thymus can have an activated
>phenotype >prior to migrationto the periphery - Bendelac, Nature 1991, 353:68).
>It is >possible that CD4+8+thymocytes which are infected with HIV does not
>favor >viralreplication. There is very goodevidence that progress to single
>positive >stage, i.e. down-modulation of eitherCD4 or CD8 on double positive
>cells, is a >random event (D. Littman - D. Mathias'sgroups, Cell-1993 April
i guess you mean the "stochastic vs instructional model here? stochastic is
_not_ looking that good at this point in time. and while in all fairness,
both models _could_ have some input/ a role, many other groups have some
very good evidence that its the instructional model functioning here.
> which does >not seem to require signalling via T cellreceptor. So it could >be
>possible >that, CD4 is shut off in HIV infected CD4+8+ T cells and ifthe >CD8+
>T cell is >positively selected (assuming positive selection signals -
>whatever they are - have no influence on viral expression?) and remain resting
>for a while, HIV infection may eventually recede or enter latency. Actually,
>hasanybody looked for frequency of CD8+ T cells with HIV proviral DNA?
>(Ihaven't yet readthe refs posted by Chad Womack)
i think actually c.savoy (sp?) posted something along those reference lines
as well, but we dont want to start him and d.perrit screaming at each other
i like the idea that you brought up about pos/neg selection and _what_ role
that may have in proviral induction, ect. when and if pos selection
increases nfkb levels, hiv binds this up (on the ltr somehow) and increases
_its_ promotion. so an il2 activated signal unfortunatly increases hiv
transcription levels. this could definatly affect the integration.
apparently the basic mechinisms/science behind hiv replication /integration
are receiving a boost in funding. so maybe we'll know some of these answers
regards ralph at ccit.arizona.edu
Ralph M. Bernstein
Dept of Micro/Immuno
University of Arizona
Ph: 602 626 2585
Fx: 602 626 2100
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